Abstract

Photorhabdus spp. are Gram negative enterobacteria which have a life cycle
involving mutualism with a nematode partner and pathogenicity towards insects.
Photorhabdus reside as intestinal symbionts of the infective juvenile (IJ) stage of
entomopathogenic nematodes of the Heterorhabditis family. The bacteria and its
nematode partner together form an insect killing (entomopathogenic) complex that
kills the soil dwelling larval stages of a wide variety of insect species. Photorhabdus
spp. have the ability to exist in either of two phenotypically different forms. The
bacterial form isolated from the nematode is referred to as the primary phenotype
variant, whilst the phenotypically different form is referred to as secondary phenotype
variant. This secondary variant is isolated after prolonged stationary phase growth of
the primary variant. The secondary variant does not support mutualism with the
nematode partner and does not produce pigment, bioluminescence, extracellular
enzymes, antibiotics and displays a different colony morphology to the primary
variant. Study of the phenotypic switch undergone by Photorhabdus has identified
two signalling pathways which play a role in the regulation of phenotypic variation -
the LysR-type transcriptional regulator HexA and the ‘adaptation to stationary phase’
AstR-AstS two component signal transduction system. A putative DNA binding
protein, Ner, has also been shown to influence the phenotypic switch when
overexpressed. This study has confirmed the role of HexA in the regulation of
symbiosis, virulence and phenotypic variation in P. temperata K122 and furthermore,
has identified a role for HexA in regulating the small RNA global regulator csrB.
Other genes, including hipB (part of a toxin/antitoxin system) and sdiA a LuxR type
regulator have also been identified as having potential roles in phenotypic variation.
A broad range of other genes that influence phenotypic variation either directly or
indirectly have also been identified, providing further insight into the reasons for the
occurrence of phenotypic variation in P. temperata K122.